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PRDX6过表达促进A549细胞在体外和体内的增殖、侵袭及迁移。

PRDX6 Overexpression Promotes Proliferation, Invasion, and Migration of A549 Cells in vitro and in vivo.

作者信息

Li Hao, Zhang Donghua, Li Bo, Zhen Honghua, Chen Wenping, Men Qingjuan

机构信息

Department of Blood Transfusion, Shandong Provincial Hospital Affiliated with Shandong First Medical University, Shandong, 271016, People's Republic of China.

Department of Oncology, Zhangqiu People's Hospital Shandong Province, Shandong, 250200, People's Republic of China.

出版信息

Cancer Manag Res. 2021 Feb 10;13:1245-1255. doi: 10.2147/CMAR.S284195. eCollection 2021.

DOI:10.2147/CMAR.S284195
PMID:33603470
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7883393/
Abstract

PURPOSE

Peroxiredoxin-6 (PRDX6) is frequently found in various cancers. However, its expression and relevance to proliferation, invasion, and migration in human non-small-cell lung cancer (NSCLC) remain unclear. This study investigated the role and novel mechanism of PRDX6 in progression in an NSCLC cell line (A549).

METHODS

We analyzed the expression of PRDX6 in NSCLC and adjacent normal tissues and explored the proliferation, migration, and invasion of A549 cells using either a PRDX6 plasmid or PRDX6 small interfering RNA (siRNA). We also assessed the effects of PRDX6 on the epithelial-mesenchymal transition (EMT) and β-catenin-mediated transcription of target genes.

RESULTS

PRDX6 expression was markedly higher in NSCLC tissues than in adjacent tissues. Proliferation, invasion, and migration of A549 cells were promoted by overexpression of PRDX6 but inhibited by its silencing. PRDX6 overexpression inhibited the protein expression of both phosphorylated β-catenin and E-cadherin, as well as the expression of vimentin, TWIST, and downstream targets of β-catenin including c-MYC, TCF-4, and MMP14. Conversely, PRDX6 silencing markedly decreased the expression of c-MYC, TCF-4, and MMP14, and inhibited EMT in A549 cells. Overexpression of PRDX6 in vivo notably increased the volume and weight of tumors.

CONCLUSION

PRDX6 overexpression promotes the proliferation, invasion, and migration of A549 cells in vitro and in vivo.

摘要

目的

过氧化物酶体增殖物激活受体6（PRDX6）在多种癌症中经常被发现。然而，其在人类非小细胞肺癌（NSCLC）中的表达及其与增殖、侵袭和迁移的相关性仍不清楚。本研究调查了PRDX6在NSCLC细胞系（A549）进展中的作用和新机制。

方法

我们分析了PRDX6在NSCLC组织和相邻正常组织中的表达，并使用PRDX6质粒或PRDX6小干扰RNA（siRNA）探索了A549细胞的增殖、迁移和侵袭。我们还评估了PRDX6对上皮-间质转化（EMT）和β-连环蛋白介导的靶基因转录的影响。

结果

PRDX6在NSCLC组织中的表达明显高于相邻组织。PRDX6的过表达促进了A549细胞的增殖、侵袭和迁移，但其沉默则抑制了这些过程。PRDX6的过表达抑制了磷酸化β-连环蛋白和E-钙黏蛋白的蛋白表达，以及波形蛋白、TWIST和β-连环蛋白下游靶标（包括c-MYC、TCF-4和MMP14）的表达。相反，PRDX6的沉默显著降低了c-MYC、TCF-4和MMP14的表达，并抑制了A549细胞中的EMT。PRDX6在体内的过表达显著增加了肿瘤的体积和重量。

结论

PRDX6的过表达促进了A549细胞在体外和体内的增殖、侵袭和迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc2/7883393/444201fc9912/CMAR-13-1245-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc2/7883393/dd77e48e9b81/CMAR-13-1245-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc2/7883393/3e4bd83c0bb0/CMAR-13-1245-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc2/7883393/af54768fc9e0/CMAR-13-1245-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc2/7883393/f06e0df408b3/CMAR-13-1245-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc2/7883393/0e279028196f/CMAR-13-1245-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc2/7883393/444201fc9912/CMAR-13-1245-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc2/7883393/dd77e48e9b81/CMAR-13-1245-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc2/7883393/3e4bd83c0bb0/CMAR-13-1245-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc2/7883393/af54768fc9e0/CMAR-13-1245-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc2/7883393/f06e0df408b3/CMAR-13-1245-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc2/7883393/0e279028196f/CMAR-13-1245-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bc2/7883393/444201fc9912/CMAR-13-1245-g0006.jpg

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